GPD1 Sheep IgG antibody Ab Biotin
- Known as:
- GPD1 Sheep Immunoglobulin G (anti-) Antibody Biotin
- Catalog number:
- AP21312BT-N
- Product Quantity:
- 1 ml
- Category:
- -
- Supplier:
- ACR
- Gene target:
- GPD1 Sheep IgG antibody Biotin
Related genes to: GPD1 Sheep IgG antibody Ab Biotin
- Gene:
- GPD1 NIH gene
- Name:
- glycerol-3-phosphate dehydrogenase 1
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 12q13.12
- Locus Type:
- gene with protein product
- Date approved:
- 2001-06-22
- Date modifiied:
- 2015-11-05
Related products to: GPD1 Sheep IgG antibody Ab Biotin
Related articles to: GPD1 Sheep IgG antibody Ab Biotin
- Productive efficiency in laying breeders is influenced by genetic and physiological factors, but it remains unclear whether maternal reproductive precocity programs distinct inflammatory responses in the offspring. This study evaluated the effects of maternal precocity on productive performance, immunological parameters, and the intestinal transcriptomic profile of Japanese quail offspring challenged with lipopolysaccharide (LPS). A design with two maternal groups was used (early-maturing: reaching 95% lay between weeks 14-15; and late-maturing: between weeks 17-18), and the offspring were either challenged or not with LPS at 25 days of age, with jejunum collection for RNA sequencing. Early-maturing dams showed better productive performance and lower stress indicators (lower heterophil:lymphocyte ratio and lower relative spleen weight) (p < 0.05). Their offspring, when challenged with LPS, exhibited a metabolic suppression profile, with downregulation of genes linked to oxidative phosphorylation (NDUFA5, NDUFS6; adj. p = 0.006 for the oxidative phosphorylation pathway), NADH metabolism (GPD1; adj. p = 0.005 for NADH metabolic process), and amino acid transport (SLC25A13, SLC25A15; adj. p = 0.005 for l-amino acid transmembrane transport), associated with activation of anti-inflammatory mediators (IL18BP, IL1R2; adj. p = 0.032 for cytokine binding), characterizing an energy-saving tolerance strategy to inflammation. In contrast, the offspring of late-maturing dams challenged with LPS showed strong activation of matrix metalloproteinase MMP7 (adj. p = 0.004 for collagen catabolic process) and exclusive enrichment of the Wnt signaling pathway (adj. p = 0.003), indicating a response directed toward extracellular matrix remodeling and tissue repair. In conclusion, maternal precocity programs two distinct transcriptional phenotypes in the offspring facing an inflammatory challenge: metabolic tolerance with immunomodulation (descendants of early-maturing dams) versus resistance with tissue remodeling (descendants of late-maturing dams), demonstrating that maternal genetic merit determines different resource allocation strategies between immune defense and homeostasis maintenance. - Source: PubMed
Publication date: 2026/08/03
Conceição Juliana Dos SantosGasparino ElianeKhatlab Angélica de SouzaBarbosa Marcos Adriano PereiraSantos Vanicleide da Silvada Silva Lucas SoaresBastos Marisa SilvaSantana Thais PachecoMarcato Simara MárciaDdine Emine Mayer ChamseZancanella Vittor TuzziBrito Claudson OliveiraVieira Jodnes SobreiraPaula Del Vesco Ana - Efficient biosynthesis of 1,3-PDO, a key bio-based chemical, depends on precise regulation of the host metabolic network. In this study, a heterologous CRISPR-Cas12a genome editing system was established and systematically optimized in Klebsiella pneumoniae, enabling efficient and stable genome editing (75-100% efficiency). Using on this platform, by-product pathways were reduced through multi-gene deletions (frdA, poxB, adhE, ldhA, glpK, ptsG and dhaM) to enhance the yield of 1,3-PDO from glycerol. By heterologously expressing GPD1/GPP2 and optimizing promoter, a metabolic network for the "glucose-glycerol-1,3-PDO" pathways was reconstructed. Cometabolism studies indicated that low concentrations of xylose and arabinose as co-substrates enhanced conversion efficiency of glycerol, whereas glucose alleviated metabolic competition. Under cometabolism of glucose and glycerol, the engineered strain K. pneumoniae S2 ΔABEAKGM-1-2 produced 1003.7 mmol/L (76.4 g/L) of 1,3-PDO with a yield of 0.83 mol/mol glycerol, an overall molar yield of 0.78 mol/mol based on total substrate consumption, and a productivity of 27.9 mmol/L/h. When lignocellulosic hydrolysate was used as co-substrate, 981.1 mmol/L (74.7 g/L) of 1,3-PDO was produced with a yield of 0.77 mol/mol glycerol and a productivity of 27.3 mmol/L/h. This study achieved efficient redirection of carbon flux toward 1,3-PDO through systematic metabolic engineering, providing valuable strain resources and technical guidance for the sustainable and cost-effective biomanufacturing of bio-based 1,3-PDO. - Source: PubMed
Publication date: 2026/09/13
Wang LiZhao MingyangYe YuanmingFeng CaiSun YaqinZhu ZhiweiYang ShihuiXiu Zhilong - Azole resistance in fungal pathogens is a growing clinical and environmental concern. However, short-term cellular responses during the first hours of azole exposure remain insufficiently characterised, particularly in filamentous fungi. This study used as a genetically tractable model to investigate early cellular responses to azole stress. Exponentially growing mycelia were exposed to conidium-derived MIC reference concentrations of fluconazole, voriconazole, ravuconazole, and ketoconazole. Early responses were assessed by monitoring radial growth, intracellular glycerol, HDCF-DA microscopy, antioxidant enzyme activities, Calcofluor White staining, and RT-qPCR analysis of genes associated with osmoregulation, sterol homeostasis, oxidative stress, and cell-wall remodelling. Azole exposure was associated with reduced net post-transfer radial growth and rapid treatment- and time-dependent changes in intracellular glycerol. Induction of together with treatment-dependent changes in and glycerol accumulation was consistent with an early osmoregulatory response. Sterol-homeostasis genes showed selective feedback regulation, and several cell-wall-remodelling genes underwent treatment-dependent transcriptional changes. Qualitative HDCF-DA microscopy showed limited oxidant-associated fluorescence during azole challenge. Catalase activity remained close to control levels, whereas representative SOD-activity experiments showed larger fold changes after voriconazole and ravuconazole exposure. Representative Calcofluor White micrographs showed irregular septation and localised regions of enhanced cell-wall-associated staining. shows multiple concurrent early responses to azole stress involving osmotic adjustment, sterol-pathway feedback, antioxidant responses, and cell-wall remodelling. These findings provide a framework for future studies examining how such stress responses contribute to recovery, tolerance, or longer-term adaptation. - Source: PubMed
Publication date: 2026/08/19
Pagáč TomášVíglaš JánOlejníková Petra - The development of uniformly distributed ultrafine metallic nanoclusters for advanced catalysts has attracted significant interest. However, synthesizing supports with specific electronic environments and well-defined pores to prevent aggregation remains challenging. Here, we report a facile palladium/copper cocatalyzed polycondensation to synthesize carbon-rich acetylenic nanostructures, poly(1,3,5-triethynylbenzene) (PTEB), for the in situ chelation of ultrafine Pd nanoclusters (∼0.4 nm). The extensive π-conjugated configuration of PTEB provides an electron-rich environment that enhances Pd coordination through charge transfer, while its intrinsic pore structures ensure exceptional Pd dispersibility and effective spatial confinement. This synergistic electronic and spatial design in Pd/PTEB catalysts exhibits impressive catalytic activities in liquid-phase reactions, achieving a remarkable turnover frequency of 15 039 molC=C molPd-1 h-1 in the semihydrogenation of 1-octyne and a rate constant of 2.26 × 107 min-1 gPd-1 for 4-nitrophenol reduction. These performances represent a significant improvement over commercial and previously reported Pd catalysts, demonstrating promising advances for stable and active heterogeneous catalysts. - Source: PubMed
Su XinyuYu FengSong HouhongWang QiangQiu ShengenLiu ZhiboYao SiyuHan GaorongRen WencaiChen ZongpingFeng Xinliang - To investigate the causal effects of antidiabetic drug targets on Bell's palsy risk using Mendelian randomization (MR), addressing limitations of observational studies and informing therapeutic strategies for diabetic patients. A 2-sample MR analysis was conducted using genetic instruments for 5 major antidiabetic drug classes: sulfonylureas (ABCC8/KCNJ11), metformin (GPD1), thiazolidinediones (PPARG), GLP1-RAs (GLP1R), and SGLTi (SLC5A1/2). Instrumental variables were selected from cis-regions (±500 kb) of target genes using HbA1c-associated single nucleotide polymorphisms (GWAS ID: ebi-a-GCST90014006) with stringent clumping (P < 5 × 10-8, r2 < 0.2) and F-statistic > 10 to ensure robustness. Bell's palsy data were sourced from FinnGen (finn-b-G6_BELLPA) including. Causal effects were assessed via inverse variance weighted, MR-Egger, and weighted median methods, complemented by sensitivity analyses (MR-Pleiotropy RESidual Sum and Outlier, Cochran's Q). Genetically proxied sulfonylurea (via ABCC8/KCNJ11) and metformin (via GPD1) targets exhibited significant protective effects against Bell's palsy, with odds ratios of 0.19 (95% CI: 0.04-0.92, P = .039) and 0.16 (0.03-0.87, P = .034), respectively. Sensitivity analyses confirmed minimal pleiotropy (MR-Egger intercept P > .05) and heterogeneity (Cochran's Q P > .05). No associations were observed for thiazolidinediones, GLP1-RAs, or SGLTi. Scatter plots and inverse variance weighted median concordance supported robustness for ABCC8/KCNJ11, though limited single nucleotide polymorphisms for GPD1 warranted cautious interpretation. This MR analysis provides genetic evidence that sulfonylureas and metformin may confer neuroprotection against Bell's palsy, supporting potential repurposing of these agents to mitigate neurological complications in diabetic patients. - Source: PubMed
Lu KaifuYe LinlinYi XuelianHe Yuxin